Tamoxifen-induced fatty liver in patients with breast cancer

Ogawa, Yasuhiro; Murata, Yoriko; Nishioka, Akihito; Inomata, Taisuke; Shoji, Yasuhiro

doi:10.1016/s0140-6736(05)78493-2

Cited by 104 publications

(65 citation statements)

References 3 publications

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“…Both human and rodent studies provide evidence for a protective effect of estrogen and testosterone on the development of fatty liver (15)(16)(17)(19)(20)(21). We set out to investigate the effect of gonadectomy in three different strains of both sexes.…”

Section: Discussionmentioning

confidence: 99%

“…Also, NAFLD has been shown to be more prevalent in post-as compared with premenopausal women, suggesting that sex hormones may influence the onset of NAFLD (15). The fact that breast cancer patients treated with an estrogen receptor antagonist develop massive hepatic steatosis and even typical NASH indicates that estrogen affects development of this disease (16). Cross-sectional studies assessing the association between plasma testosterone and NAFLD have shown conflicting results (17)(18)(19).…”

Section: Accession Numbersmentioning

confidence: 99%

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Genetic and hormonal control of hepatic steatosis in female and male mice

Norheim

Hui

Kulahcioglu

et al. 2017

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Section: Accession Numbersmentioning

confidence: 99%

Genetic and hormonal control of hepatic steatosis in female and male mice

Norheim

Hui

Kulahcioglu

et al. 2017

Journal of Lipid Research

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“…In a large crosssectional study in men, low E 2 was associated with the presence of hepatic steatosis (48). Furthermore, tamoxifen when used as an adjuvant chemotherapeutic agent in patients with breast cancer is known to be associated with NAFLD (49).…”

Section: Oestrogensmentioning

confidence: 98%

Mechanisms in endocrinology: Non-alcoholic fatty liver disease in common endocrine disorders

Hazlehurst

Tomlinson

2013

European Journal of Endocrinology

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Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disease spanning from simple benign steatosis to steatohepatitis with fibrosis and scarring that can eventually lead to cirrhosis. Its prevalence is rising rapidly and is developing into the leading indication for liver transplantation worldwide. Abnormalities in endocrine axes have been associated with NALFD, including hypogonadism, hypothyroidism, GH deficiency and hypercortisolaemia. In some instances, correction of the endocrine defects has been shown to have a beneficial impact. While in patients with type 2 diabetes the association with NAFLD is well established and recognised, there is a more limited appreciation of the condition among common endocrine diseases presenting with hormonal excess or deficiency. In this review, we examine the published data that have suggested a mechanistic link between endocrine abnormalities and NAFLD and summarise the clinical data endorsing these observations.

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“…As GH stimulates hepatic triglyceride export and fatty acid oxidation, the inhibitory effect on hepatic GH action by SERMS may lead to suppress hepatic lipid metabolism resulting in liver steatosis development [52,74,78,79]. Fatty liver development is a risk of tamoxfen therapy in women with breast cancer [80]. In contrast to SERMs, fatty liver is not an adverse effect of aromatase inhibitors as they do not affect hepatic GH action.…”

Section: A C C E P T E Dmentioning

confidence: 99%

Sex steroids and the GH axis: Implications for the management of hypopituitarism

Birzniece

2017

Best Practice & Research Clinical Endocrinology & Metab

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Growth hormone (GH) regulates somatic growth, substrate metabolism and body composition. Sex hormones exert profound effect on the secretion and action of GH.Estrogens stimulate the secretion of GH, but inhibit the action of GH on the liver, an effect that occurs when administered orally. Estrogens suppress GH receptor signaling by stimulating the expression proteins that inhibit cytokine receptor signaling. This effect of estrogens is avoided when physiological doses of estrogens are administered via a non-oral route. Estrogen-like compounds, such as selective estrogen receptor modulators, possess dual properties of inhibiting the secretion as well as the action of GH. In contrast, androgens stimulate GH secretion, driving IGF-1 production. In the periphery, androgens enhance the action of GH. The differential effects of estrogens and androgens influence the dose of GH replacement in patients with hypopituitarism on concomitant treatment with sex steroids.Where possible, a non-oral route of estrogen replacement is recommended for optimising cost-benefit of GH replacement in women with GH deficiency. Adequate androgen replacement in conjunction with GH replacement is required to achieve the full anabolic effect in men with hypopituitarism.

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Tamoxifen-induced fatty liver in patients with breast cancer

Cited by 104 publications

References 3 publications

Genetic and hormonal control of hepatic steatosis in female and male mice

Genetic and hormonal control of hepatic steatosis in female and male mice

Mechanisms in endocrinology: Non-alcoholic fatty liver disease in common endocrine disorders

Sex steroids and the GH axis: Implications for the management of hypopituitarism

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